Differentially expressed genes between high-risk human papillomavirus types in human cervical cancer cells

Abstract

Cervical carcinoma (CC) is one of the most common cancers among women worldwide and the first cause of death among the Mexican female population. Human papillomavirus (HPV) infection is the most important etiologic factor for CC. Of the oncogenic types, HPV16 and HPV18 are found in 60-70% of invasive CCs worldwide. HPV18 appears to be associated with a more aggressive form of cervical neoplasia than HPV16 infection. At present, there are no studies on differentially expressed cellular genes between transformed cells harboring HPV16 and HPV18 sequences. Based on previous complementary DNA microarray data from our group, 13 genes were found to be differentially overexpressed between HPV16- and HPV18-transformed cells. These genes were as follows: E6BP, UBE4A, C20orf14, ATF7, ABCC8, SLC6A12, WASF3, SUV39H1, SPAG8, CCNC, E2FFE, BIRC5, and DEDD. Differential expression of six selected genes was confirmed by real-time reverse transcription-polymerase chain reaction (RT-PCR). All real-time RT-PCRs confirmed differential expression between HPV18 and HPV(-) samples. The present work identifies genes from signaling pathways triggered by HPV transformation that could be differentially deregulated between HPV16(+) and HPV18(+) samples.

The human papillomavirus E7 oncoprotein as a regulator of transcription

“…In addition, differentiation-related genes (Nees, Geoghegan et al 2000; Johung, Goodwin et al 2007; Gyongyosi, Szalmas et al 2014), innate immune response genes (Chang and Laimins 2000; Nees, Geoghegan et al 2001; Cortes-Malagon, Bonilla-Delgado et al 2013; Zhou, Zhang et al 2016), DNA damage and stress response genes (Zhou, Zhang et al 2016), and growth factors (Nees, Geoghegan et al 2000) have appeared repeatedly. In studies that take differentiation into account, E7 has been found to have a more profound effect in differentiating cells than in undifferentiated cells (Nees, Geoghegan et al 2001; Vazquez-Ortiz, Garcia et al 2007). …”

Analysis of Argonaute Complex Bound mRNAs in DU145 Prostate Carcinoma Cells Reveals New miRNA Target Genes

“…DEDD can attenuate epithelial-mesenchymal transition and acts as an endogenous suppressor of tumor growth and metastasis in human breast cancer [51]. However, overexpression of DEDD was observed in HP16/18 transformed cervical carcinoma cells [52]. Also copy number gain of 1q23.3 which included amplification of DEDD in urothelial tumors was recently described [53] as well as increased DEDD expression in nasopharyngeal carcinoma [54].…”

Matrix metalloproteinases 2 and 9, their endogenous regulators, and angiotensin-converting enzyme in cervical squamous cell carcinoma

“…Этиологическими факторами возникно-вения РШМ служат вирусы папиллом (HPV) высокого ри-ска, среди которых вирусы HPV16 и HPV18 являются наи-более распространенными и агрессивными [11]. В случае карциномы шейки матки имеются немногочисленные дан-ные об увеличении экспрессии желатиназ А и В в опухоли, а также данные об экспрессии ТИМП-2 [12].…”